Mammalian embryogenesis is a process which encompasses the first few weeks of development following conception. During this period, embryogenesis proceeds from a single fertilized egg cell to the formation of the three embryonic tissues, then to an embryo which has most of its internal organs and all of its external features.
The normal course of mammalian embryogenesis depends on the correct temporal and spatial regulation of a large number of genes and tissues. These regulation processes have been intensely studied using transgenic mice. Integration of retroviral or other nucleic acids into the mouse germ line often disrupts a mouse gene at the point of insertion and produces mutations which correlate with developmental abnormalities. One such mutation has been identified as recessive H.beta.58 (Radice, G. et al. (1991) Development 111:801-811). Homozygous H.beta.58 embryos display abnormalities such as reduced embryonic ectoderm, abnormal folding of amnion and chorion tissues due to over-proliferation, and failure of allantois and chorion to form a proper placenta. These phenotypic characteristics suggest that the mouse gene inactivated by the H.beta.58 insertion is involved in the development of the embryonic ectoderm (Radice et al., supra).
The H.beta.58 gene encodes a 38 kDa H.beta.58 protein. In situ hybridization shows that expression of the wild-type H.beta.58 gene begins in the oocyte and continues throughout pre- and post-implantation embryogenesis. In early post-implantation embryos, H.beta.58 expression is low in embryonic ectoderm and high in visceral endoderm. Even though phenotypic effects of the mutation are displayed in the embryonic ectoderm, these results suggest that the effects of the mutation may be exerted indirectly via the visceral endoderm (Lee, J. J. et al. (1992) Development 115: 277-288).
The discovery of a new human embryogenesis protein and the polynucleotides encoding it satisfies a need in the art by providing new compositions which are useful in the diagnosis, prevention and treatment of disorders associated with cell proliferation and apoptosis.